Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs
Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs
Combined Automated Annotation using Multiple IEA Methods
Hepatocyte nuclear factor-1alpha is an essential regulator of bile acid and plasma cholesterol metabolism.
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Mouse hepatic Slc10a1 is a basolateral membrane bile acid transporter whose reduced expression impairs portal bile acid uptake and elevates plasma bile acid concentrations.
"Tcf1-/- liver has decreased expression of the basolateral membrane bile acid transporters Slc10a1, Slc21a3 and Slc21a5, leading to impaired portal bile acid uptake and elevated plasma bile acid concentrations."
Molecular cloning and functional characterization of two alternatively spliced Ntcp isoforms from mouse liver1.
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Mouse Ntcp was cloned as two alternatively spliced isoforms, a 362-residue form and a C-terminally shortened 317-residue form.
"we screened a mouse liver cDNA library and identified Ntcp1, encoding a 362 amino acid protein and Ntcp2, encoding a 317 amino acid protein which had a shorter C-terminal end."
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Both mouse Ntcp isoforms mediate saturable, sodium-dependent taurocholate transport in Xenopus oocytes.
"Both isoforms mediated saturable Na+-dependent transport of taurocholate when expressed in Xenopus laevis oocytes."
Functional and Pharmacological Comparison of Human and Mouse Na(+)/Taurocholate Cotransporting Polypeptide (NTCP).
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NTCP is located in the basolateral membrane of hepatocytes and transports bile acids from portal blood into the hepatocyte.
"The Na+/taurocholate cotransporting polypeptide (NTCP) is located in the basolateral membrane of hepatocytes, where it transports bile acids from the portal blood back into hepatocytes."
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Mouse Ntcp and human NTCP have closely similar affinities for estrone-3-sulfate and for the drug rosuvastatin.
"a functional comparison of human NTCP (hNTCP) and mouse Ntcp (mNtcp) showed similar Km values of 67 ± 10 µM and 104 ± 9 µM for the probe substrate estrone-3-sulfate as well as of 258 ± 42 µM and 199 ± 13 µM for the drug rosuvastatin, respectively."
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NTCP contributes to hepatic transport of drugs.
"Furthermore, NTCP has a role for the hepatic transport of some drugs."
Molecular determinants of hepatitis B and D virus entry restriction in mouse sodium taurocholate cotransporting polypeptide.
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Mouse Ntcp cannot support HBV or HDV infection, although it binds the preS1 domain of the HBV L protein and transports taurocholate normally.
"mNTCP was found to be unable to support either HBV or HDV infection, although it can bind to pre-S1 of HBV L protein and is functional in transporting substrate taurocholate"
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Expression of mouse Ntcp fails to render HepG2 cells susceptible to HBV or HDV, matching the host restriction seen in mice.
"mNTCP failed to render HepG2 susceptible for HDV or HBV infection, a finding consistent with the host restriction in mouse."
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Replacing mouse Ntcp residues 84-87 with their human counterparts converts it into a functional HBV/HDV receptor, localizing the restriction to the first extracellular loop.
"Remarkably, when mNTCP residues 84 to 87 were substituted by human counterparts, mNTCP can effectively support viral infections."
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The restriction is not a transport defect; mouse Ntcp mediates sodium-dependent taurocholate uptake as efficiently as human NTCP.
"In addition, mNTCP can mediate taurocholate uptake in the presence of sodium as efficient as hNTCP"
Sodium taurocholate cotransporting polypeptide is a functional receptor for human hepatitis B and D virus.
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Human NTCP is necessary and sufficient for HBV and HDV entry in cultured hepatocarcinoma cells.
"Silencing NTCP inhibited HBV and HDV infection, while exogenous NTCP expression rendered nonsusceptible hepatocarcinoma cells susceptible to these viral infections."